Journal articles: 'ArnA Protein'

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Kopp, Ulla C., Donna M. Farley, Michael Z. Cicha, and Lori A. Smith. "Activation of renal mechanosensitive neurons involves bradykinin, protein kinase C, PGE2, and substance P." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 4 (April 1, 2000): R937—R946. http://dx.doi.org/10.1152/ajpregu.2000.278.4.r937.

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Increased renal pelvic pressure or bradykinin increases afferent renal nerve activity (ARNA) via PGE2-induced release of substance P. Protein kinase C (PKC) activation increases ARNA, and PKC inhibition blocks the ARNA response to bradykinin. We now examined whether bradykinin mediates the ARNA response to increased renal pelvic pressure by activating PKC. In anesthetized rats, the ARNA responses to increased renal pelvic pressure were blocked by renal pelvic perfusion with the bradykinin B2-receptor antagonist HOE 140 and the PKC inhibitor calphostin C by 76 ± 8% ( P < 0.02) and 81 ± 5% ( P < 0.01), respectively. Renal pelvic perfusion with 4β-phorbol 12,13-dibutyrate (PDBu) to activate PKC increased ARNA 27 ± 4% and renal pelvic release of PGE2 from 500 ± 59 to 1,113 ± 183 pg/min and substance P from 10 ± 2 to 30 ± 2 pg/min (all P < 0.01). Indomethacin abolished the increases in substance P release and ARNA. The PDBu-mediated increase in ARNA was also abolished by the substance P-receptor antagonist RP 67580. We conclude that bradykinin contributes to the activation of renal pelvic mechanosensitive neurons by activating PKC. PKC increases ARNA via a PGE2-induced release of substance P.

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Marcos, Caroline Maria, Haroldo Cesar de Oliveira, Patricia Akemi Assato, Cleverton Roberto de Andrade, Ana Marisa Fusco-Almeida, and Maria José Soares Mendes-Giannini. "Paracoccidioides brasiliensis 14-3-3 protein is important for virulence in a murine model." Medical Mycology 57, no. 7 (November 24, 2018): 900–904. http://dx.doi.org/10.1093/mmy/myy112.

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AbstractThe Paracoccidioides brasiliensis strain downregulated the expression of adhesin Pb14-3-3 (Pb14-3-3 aRNA) was evaluated in a murine model of paracoccidioidomycosis (PCM). Pb14-3-3 aRNA displays attenuated virulence and triggered the formation of fewer granulomas by lowering the fungal burden in the lungs. Additionally, the Pb14-3-3 aRNA showed more elongated yeast cells and less ability to induce pneumocytes apoptosis in vitro. Our results show that 14-3-3 is an important virulence factor in P. brasiliensis-induced pulmonary infection.

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Kopp, U. C., and L. A. Smith. "A role for protein kinase C in bradykinin-mediated activation of renal pelvic sensory receptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 269, no. 2 (August 1, 1995): R331—R338. http://dx.doi.org/10.1152/ajpregu.1995.269.2.r331.

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In anesthetized rats, activation of renal pelvic sensory receptors by bradykinin results in an increase in afferent renal nerve activity (ARNA) that is dependent on intact renal prostaglandin synthesis. Since bradykinin is a known activator of the phosphoinositide system, we examined whether the increase in ARNA produced by bradykinin involved activation of protein kinase C (PKC). Renal pelvic perfusion with the phorbol ester 4 beta-phorbol 12,13-dibutyrate (PDBu, 1 microM) increased ARNA (31 +/- 3%, P < 0.01) in rats fed a normal diet but not in rats fed an essential fatty acid-deficient (EFAD) diet. Renal pelvic perfusion with the PKC inhibitors calphostin C (1 microM), staurosporine (20 nM), and H-7 (40 microM) reduced the ARNA responses to bradykinin (20 microM) by 69 +/- 10, 76 +/- 10, and 77 +/- 10%, respectively (all P < 0.01). Pretreatment with PDBu (1 microM), known to cause a feedback inhibition of bradykinin-mediated activation of the phosphoinositide system, reduced the ARNA response to bradykinin by 73 +/- 6% (P < 0.01). Pretreatment with 4 alpha-phorbol 12,13-didecanoate was without effect. These findings suggest that activation of PKC contributes importantly to the activation of renal pelvic sensory receptors by bradykinin, likely via release of arachidonic acid.

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Fischer, Utz, Simon Hertlein, and Clemens Grimm. "The structure of apo ArnA features an unexpected central binding pocket and provides an explanation for enzymatic cooperativity." Acta Crystallographica Section D Biological Crystallography 71, no. 3 (February 26, 2015): 687–96. http://dx.doi.org/10.1107/s1399004714026686.

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The bacterial protein ArnA is an essential enzyme in the pathway leading to the modification of lipid A with the pentose sugar 4-amino-4-deoxy-L-arabinose. This modification confers resistance to polymyxins, which are antibiotics that are used as a last resort to treat infections with multiple drug-resistant Gram-negative bacteria. ArnA contains two domains with distinct catalytic functions: a dehydrogenase domain and a transformylase domain. The protein forms homohexamers organized as a dimer of trimers. Here, the crystal structure of apo ArnA is presented and compared with its ATP- and UDP-glucuronic acid-bound counterparts. The comparison reveals major structural rearrangements in the dehydrogenase domain that lead to the formation of a previously unobserved binding pocket at the centre of each ArnA trimer in its apo state. In the crystal structure, this pocket is occupied by a DTT molecule. It is shown that formation of the pocket is linked to a cascade of structural rearrangements that emerge from the NAD+-binding site. Based on these findings, a small effector molecule is postulated that binds to the central pocket and modulates the catalytic properties of ArnA. Furthermore, the discovered conformational changes provide a mechanistic explanation for the strong cooperative effect recently reported for the ArnA dehydrogenase function.

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Kopp, Ulla C., Olaf Grisk, Michael Z. Cicha, Lori A. Smith, Antje Steinbach, Torsten Schlüter, Nicole Mähler, and Tomas Hökfelt. "Dietary sodium modulates the interaction between efferent renal sympathetic nerve activity and afferent renal nerve activity: role of endothelin." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, no. 2 (August 2009): R337—R351. http://dx.doi.org/10.1152/ajpregu.91029.2008.

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Increasing efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA), which in turn decreases ERSNA via activation of the renorenal reflexes in the overall goal of maintaining low ERSNA. We now examined whether the ERSNA-induced increases in ARNA are modulated by dietary sodium and the role of endothelin (ET). The ARNA response to reflex increases in ERSNA was enhanced in high (HNa)- vs. low-sodium (LNa) diet rats, 7,560 ± 1,470 vs. 900 ± 390%·s. The norepinephrine (NE) concentration required to increase PGE2 and substance P release from isolated renal pelvises was 10 pM in HNa and 6,250 pM in LNa diet rats. In HNa diet pelvises 10 pM NE increased PGE2 release from 67 ± 6 to 150 ± 13 pg/min and substance P release from 6.7 ± 0.8 to 12.3 ± 1.8 pg/min. In LNa diet pelvises 6,250 pM NE increased PGE2 release from 64 ± 5 to 129 ± 22 pg/min and substance P release from 4.5 ± 0.4 to 6.6 ± 0.7 pg/min. In the renal pelvic wall, ETB-R are present on unmyelinated Schwann cells close to the afferent nerves and ETA-R on smooth muscle cells. ETA-receptor (R) protein expression in the renal pelvic wall is increased in LNa diet. In HNa diet, renal pelvic administration of the ETB-R antagonist BQ788 reduced ERSNA-induced increases in ARNA and NE-induced release of PGE2 and substance P. In LNa diet, the ETA-R antagonist BQ123 enhanced ERSNA-induced increases in ARNA and NE-induced release of substance P without altering PGE2 release. In conclusion, activation of ETB-R and ETA-R contributes to the enhanced and suppressed interaction between ERSNA and ARNA in conditions of HNa and LNa diet, respectively, suggesting a role for ET in the renal control of ERSNA that is dependent on dietary sodium.

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Robichon, Carine, Jianying Luo, Thomas B. Causey, Jack S. Benner, and James C. Samuelson. "Engineering Escherichia coli BL21(DE3) Derivative Strains To Minimize E. coli Protein Contamination after Purification by Immobilized Metal Affinity Chromatography." Applied and Environmental Microbiology 77, no. 13 (May 20, 2011): 4634–46. http://dx.doi.org/10.1128/aem.00119-11.

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ABSTRACTRecombinant His-tagged proteins expressed inEscherichia coliand purified by immobilized metal affinity chromatography (IMAC) are commonly coeluted with nativeE. coliproteins, especially if the recombinant protein is expressed at a low level. TheE. colicontaminants display high affinity to divalent nickel or cobalt ions, mainly due to the presence of clustered histidine residues or biologically relevant metal binding sites. To improve the final purity of expressed His-tagged protein, we engineeredE. coliBL21(DE3) expression strains in which the most recurring contaminants are either expressed with an alternative tag or mutated to decrease their affinity to divalent cations. The current study presents the design, engineering, and characterization of twoE. coliBL21(DE3) derivatives, NiCo21(DE3) and NiCo22(DE3), which express the endogenous proteins SlyD, Can, ArnA, and (optionally) AceE fused at their C terminus to a chitin binding domain (CBD) and the protein GlmS, with six surface histidines replaced by alanines. We show that eachE. coliCBD-tagged protein remains active and can be efficiently eliminated from an IMAC elution fraction using a chitin column flowthrough step, while the modification of GlmS results in loss of affinity for nickel-containing resin. The “NiCo” strains uniquely complement existing methods for improving the purity of recombinant His-tagged protein.

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Sonawane, Kailas D., Rishikesh S. Parulekar, Radhika S. Malkar, Pranhita R. Nimbalkar, Sagar H. Barage, and Deepak B. Jadhav. "Homology modeling and molecular docking studies of ArnA protein from Erwinia amylovora: role in polymyxin antibiotic resistance." Journal of Plant Biochemistry and Biotechnology 24, no. 4 (November 20, 2014): 425–32. http://dx.doi.org/10.1007/s13562-014-0293-3.

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Liu, Yifei. "Preparation of SARS-CoV-2 Polymerase Nsp12 and Optimization of Expression Conditions." Sustainability in Environment 8, no. 1 (January 23, 2023): p26. http://dx.doi.org/10.22158/se.v8n1p26.

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he core component of transcription and replication of SARS-CoV-2 is Nsp12, a non-structural protein that function as an RNA-dependent RNA polymerase. Nsp12 is a key drug target for the development of anti-coronavirus drugs. The purpose of this study was to explore and optimize the expression conditions of Nsp12 of SARS-CoV-2 with the aim of establishing expression conditions to obtain high-purity Nsp12 protein. This study compared the “ice-water bath cooling” and “shaking table cooling” methods and explored the differences in cooling rates and protein expression and properties using the two cooling methods. The shaking table cooling method resulted in reduced amounts of ArnA protein in the Nsp12 protein samples compared with levels from the ice-water bath cooling method. The shaking table method enabled purification of high-quality Nsp12 protein and ensured stable output of the protein. These methods will enable subsequent exploration of the SARS-CoV-2 replication mechanism, the development of specific drugs and drug screening for anti-SARS-CoV-2 pneumonitis.

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Ma, Ming-Chieh, Ho-Shiang Huang, Chiang-Ting Chien, Ming-Shiou Wu, and Chau-Fong Chen. "Temporal decrease in renal sensory responses in rats after chronic ligation of the bile duct." American Journal of Physiology-Renal Physiology 283, no. 1 (July 1, 2002): F164—F172. http://dx.doi.org/10.1152/ajprenal.00231.2001.

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Renal responses to renal sensory receptor activation were examined in rats after 1 and 4 wk of common bile duct ligation (CBDL). Compared with sham-operated rats (Sham), urine and sodium excretion after acute saline loading was significantly reduced at both times after CBDL. The blunted excretory responses in CBDL rats, accompanied by less activation of afferent renal nerve activity (ARNA), were already apparent at 1 wk and became severe at 4 wk. The defect in ARNA activation in CBDL rats was further studied using specific stimuli to activate renal sensory receptors. Graded increases in intrapelvic pressure or renal pelvic perfusion of substance P (SP) elicited an increase in ARNA in Sham rats, these responses being temporally attenuated in CBDL rats. Despite no significant change in renal pelvic SP release, no renorenal reflex was demonstrable in 4-wk CBDL rats. Immunoblotting showed that expression of renal pelvic neurokinin 1 (NK-1) receptors was 32 and 47% lower in 1- and 4-wk CBDL rats, respectively, than in Sham rats, this decrease correlating well with plasma SP levels. The quantitative real-time RT-PCR showed similar levels of NK-1 receptor mRNA in the renal pelvis in the Sham and 4-wk CBDL groups. We conclude that impairment of renal excretory and sensory responses increases with the duration of cirrhosis. An impaired renorenal reflex in cirrhotic rats is involved in the defective activation of the renal sensory receptors could be due, in part, to the low expression of NK-1 receptors, which is dependent on the duration of CBDL. The decrease in NK-1 receptor protein levels is not due to a decrease in mRNA levels.

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Hernández, Orville, Agostinho J. Almeida, Angel Gonzalez, Ana Maria Garcia, Diana Tamayo, Luz Elena Cano, Angela Restrepo, and Juan G. McEwen. "A 32-Kilodalton Hydrolase Plays an Important Role in Paracoccidioides brasiliensis Adherence to Host Cells and Influences Pathogenicity." Infection and Immunity 78, no. 12 (September 27, 2010): 5280–86. http://dx.doi.org/10.1128/iai.00692-10.

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ABSTRACT One of the most crucial events during infection with the dimorphic fungus Paracoccidioides brasiliensis is adhesion to pulmonary epithelial cells, a pivotal step in the establishment of disease. In this study, we have evaluated the relevance of a 32-kDa protein, a putative adhesion member of the haloacid dehalogenase (HAD) superfamily of hydrolases, in the virulence of this fungus. Protein sequence analyses have supported the inclusion of PbHad32p as a hydrolase and have revealed a conserved protein only among fungal dimorphic and filamentous pathogens that are closely phylogenetically related. To evaluate its role during the host-pathogen interaction, we have generated mitotically stable P. brasiliensis HAD32 (PbHAD32) antisense RNA (aRNA) strains with consistently reduced gene expression. Knockdown of PbHAD32 did not alter cell vitality or viability but induced morphological alterations in yeast cells. Moreover, yeast cells with reduced PbHAD32 expression were significantly affected in their capacity to adhere to human epithelial cells and presented decreased virulence in a mouse model of infection. These data support the hypothesis that PbHad32p binds to extracellular matrix (ECM) proteins and modulates the initial immune response for evasion of host defenses. Our findings point to PbHAD32 as a novel virulence factor active during the initial interaction with host cells in P. brasiliensis.

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Ma, Ming-Chieh, Ho-Shiang Huang, and Chau-Fong Chen. "Impaired Renal Sensory Responses after Unilateral Ureteral Obstruction in the Rat." Journal of the American Society of Nephrology 13, no. 4 (April 2002): 1008–16. http://dx.doi.org/10.1681/asn.v1341008.

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ABSTRACT. Renal responses to the activation of renal sensory receptors were examined in rats after release of 24-h unilateral ureteral obstruction of the left kidney. The integrity of the renorenal reflex was examined in both 24-h unilateral ureteral obstruction-treated (UUO) and sham-operated (Sham) rats. Increased ipsilateral afferent renal nerve activity (ARNA) and reflexly decreased efferent renal nerve activity (ERNA) and increased contralateral diuresis and natriuresis produced by increasing the left intrapelvic pressure were observed in Sham rats but not in UUO rats. The lack of responsiveness of the renorenal reflex in UUO rats was associated with lower release of substance P (SP) and increased neutral endopeptidase (NEP) activity in the renal pelvis in the postobstructive kidney. Compared with Sham rats, urine and sodium excretion after acute saline loading was significantly reduced in the postobstructive kidney. The blunted excretory responses were accompanied by lower activation of ARNA and less reflex inhibition of ERNA. Renal sensory dysfunction in the postobstructive kidney was further examined by stimulation of renal mechanoreceptors and chemoreceptors. Graded increases in intrapelvic pressure or renal pelvic perfusion with hypertonic saline solution elicited, respectively, a pressure- or concentration-dependent increase in ARNA in the control kidney of Sham rats, this response being greatly attenuated in the postobstructive kidney. Western blots showed no quantitative difference in the expression of renal pelvic neurokinin 1 (NK-1) receptors between the two groups. It was concluded that renal sensory function is impaired in the postobstructive kidney of UUO rats and that this defective activation of renal sensory receptors results in an impaired renorenal reflex, which is associated with enhanced NEP activity and catabolism of SP released in the renal pelvis and is not related to the expression of NK-1 receptor protein.

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Suryaningrum, Theresia Dwi, Ijah Muljanah, and Evi Tahapari. "Profil Sensori dan Nilai Gizi Beberapa Jenis Ikan Patin dan Hibrid Nasutus." Jurnal Pascapanen dan Bioteknologi Kelautan dan Perikanan 5, no. 2 (November 10, 2010): 153. http://dx.doi.org/10.15578/jpbkp.v5i2.419.

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Penelitian mengenai profil sensori dan nilai gizi filet patin Siam (Pangasius hypopthalmus), Jambal (Pangasius djambal Bleeker), Pasupati, Nasutus serta hasil silangan Siam dan Nasutus (hibrid Nasutus) telah dilakukan. Analisis sensori dilakukan dengan uji pembeda menyeluruh, uji pembeda atribut, uji kesukaan, dan uji rangking. Pengamatan lainnya dilakukan terhadap edible portion dan nilai gizi (proksimat dan profil asam amino). Hasil penelitian menunjukkan bahwa filet patin hibrid Nasutus lebih memiliki kesamaan warna dengan filet patin Nasutus daripada filet patin Siam. W arna daging filet patin hibrid Nasutus berbeda nyata dengan induknya yaitu patin Nasutus dan patin Siam. Panelis lebih menyukai warna filet patin hibrid Nasutus dibandingkan dengan patin Pasupati. Patin hibrid Nasutus mempunyai tekstur yang berbeda nyata dengan Nasutus dan Jambal yang kompak dan padat, tetapi mempunyai kesamaan dengan patin Siam dan Pasupati yang agak kompak dan agak padat. Berdasarkan intensitas warna, hasil uji pembeda atribut dan uji kesukaan, maka secara berturut-turut panelis menyukai filet patin Jambal, Nasutus, hibrid Nasutus, Pasupati, dan Siam. Hibrid Nasutus mempunyai edible portionpaling tinggi (49%) dibandingkan dengan patin lainnya tetapi mempunyai kadar air, kadar lemak, dan kadar protein yang lebih rendah dan berbeda nyata dengan induknya (patin Siam dan Nasutus). Patin Siam mengandung asam amino esensial paling tinggi di antara berbagai jenis patin yang diteliti. Profil asam amino patin hibrid Nasutus, Jambal, Pasupati, dan Nasutus hampir sama, kecuali pada patin Siam yang mengandung glisin, leusin, isoleusin, histidin, serin, treonin, dan prolin yang lebih tinggi dibandingkan dengan patin lainnya

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Bluth, Martin H., Mark J. Bluth, Christopher Johns, Sohail Khan, Yin Yao Lin, Michael E. Zenilman, and Wellman Cheung. "PERIPHERAL BLOOD MONONUCLEAR CELL GENE ARRAY PROFILES IN PATIENTS WITH OVERACTIVE BLADDER (132.8)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S246—S247. http://dx.doi.org/10.4049/jimmunol.178.supp.132.8.

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Abstract Introduction: Overactive bladder (OAB) confirmation of disease often requires invasive approaches. We have previously demonstrated that peripheral blood mononuclear cells (PBMC) can provide a reporter function in solid organ retroperitoneal disease. Here we investigated the utility of using PBMC as a marker for patients with OAB. Methods: 21 patients were assessed for OAB and structural integrity. Patients with a history of recent surgery or infection were excluded. Whole blood was obtained from patients and appropriately matched controls (n=6) and PBMC were separated by density centrifugation. RNA was isolated from PBMC and converted to aRNA and subjected to microarray analysis (human U133A 2.0). Results: Microarray analysis revealed that 16 genes were differentially regulated (8 upregulated and 8 downregulated) in all patients with OAB compared with controls. Sex based analysis demonstrated 74 genes differentially regulated in males (25 upregulated and 49 downregulated), and 30 in females (13 upregulated and 17 downregulated). Of these, PDGF, MFAP3L, a microfibrillar-associated protein, and TPM1 (tropomyosin) were downregulated in all sets analyzed. Conclusions: Microarray analysis revealed many genes which were differentially regulated in PBMC from OAB patients, including regulatory/structural genes; PDGF, MFAP and TPM1 may be important in regulating structural integrity of bladder and supporting tissues. These data suggest that blood derived leukocytes can provide a reporter function for patients with solid organ disease and may serve as a diagnostic marker and/or monitor response to therapy.

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Tuñón, I., E. Silla, and J. L. Pascual-Ahuir. "Molecular surface area and hydrophobic effect." "Protein Engineering, Design and Selection" 5, no. 8 (1992): 715–16. http://dx.doi.org/10.1093/protein/5.8.715.

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Kurochkina, N., and B. Lee. "Hydrophobic potential by pairwise surface area sum." "Protein Engineering, Design and Selection" 8, no. 5 (1995): 437–42. http://dx.doi.org/10.1093/protein/8.5.437.

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Song, Lu, Kathleen A. Kelly, and Anthony W. Butch. "Monoclonal and Polyclonal Immunoglobulin Interference in a Conjugated Bilirubin Assay." Archives of Pathology & Laboratory Medicine 138, no. 7 (July 1, 2014): 950–54. http://dx.doi.org/10.5858/arpa.2013-0042-oa.

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Context.—Monoclonal proteins can interfere with the conjugated bilirubin assay on the Beckman Coulter AU5400 and AU2700 instruments and produce spurious results. Protein depletion eliminates the interference, suggesting that monoclonal proteins cause the problem. Objectives.—To determine the interference rate with the Beckman Coulter AU5400 and AU2700 conjugated bilirubin assay and to identify the interfering substance. Design.—Beckman Coulter bilirubin results from 33 720 samples analyzed during 6 months were evaluated for interference. On a subset of samples, protein G columns were used to specifically remove immunoglobulin G (IgG) to determine the cause of the interference. Another 117 samples containing a (known) monoclonal protein were selected to determine the interference rate. Results.—From 26 different patients, 103 samples had conjugated bilirubin results greater than the total bilirubin for a false-positive rate of 0.3%. Removal of IgG from a subset of those samples with IgG monoclonal protein and increased polyclonal IgG eliminated the conjugated bilirubin interference. In separate, selected samples containing monoclonal proteins, the false-positive interference rate was 7.7% (9 of 117) and was greatest when the monoclonal protein concentration was greater than 4 g/dL. Another 11 of the 117 samples (9.4%) with monoclonal proteins exhibited assay interference by producing false-negative results. The overall interference rate, therefore, was 17.1%. Conclusion.—The false-positive interference rate for the Beckman Coulter conjugated bilirubin assay was 0.3% for routinely analyzed serum/plasma samples. In addition to monoclonal proteins, we found that polyclonal immunoglobulins can also interfere with the conjugated bilirubin assay. The overall interference rate was 17.1% for samples with a monoclonal protein.

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KUSHANOVA, RZH, AA BAIDYUSSEN, GA SEREDA, SA JATAYEV, and TG SEREDA. "SPRING BARLEY HYBRIDS ASSESSMENT FOR BIOLOGICAL AND ECONOMIC FEATURES UNDER DROUGHT CONDITIONS OF NORTHERN AND CENTRAL KAZAKHSTAN." SABRAO Journal of Breeding and Genetics 55, no. 3 (June 30, 2023): 850–63. http://dx.doi.org/10.54910/sabrao2023.55.3.20.

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The presented study comprehensively assessed barley (Hordeum vulgare L.) hybrid populations of F3– F5 generations, comparing with the standard barley cultivars, Karagaydinckiy-5 and Astana-2000. The crossing of isolated barley cultivars of the international collection (obtained from Australia) proceeded under intense continental climatic conditions of Northern and Central Kazakhstan. Barley promising selected populations, i.e., Macguarie × Arna, Flinders × Tselinniy golozerniy, and Flinders × Omskiy golozerniy, showed early maturity (79–83 days), superior plant height (34.4–69.5 cm), and enhanced 1000-grain weight (56.6 g, 56.4 g, and 58.0 g, respectively), and populations, viz., Buloke × Karagandinckiy-6, Fathom × Donezckiy-9, and Onslow × Karabalykckiy-43, for productivity (1 m2) at 184 g, 116.4 g, and 140.1 g, respectively. Identified in the study were the correlation of productivity and its structural elements, particularly the grain weight per ear (r = 0.486) and grain weight per plant (r = 0.828), mainly determining grain productivity. The determination of structural features variation showed a significant excess (more than 20%) with varying levels. The level of variability of grain mass per plant has shown in hybrid lines, i.e., Fathom × Karagandinckiy-5, Onslow × Karagandinckiy-10, Admiral × Karabalykckiy-150, and Admiral × Donezckiy-9. In grains, the protein content ranged from 10.45% to 16.63%, and the excess over the standard cultivar resulted in the hybrid lines Franklin × Sabir (16.63%), Anodolu-86 × Donezckiy-8 (16.04%), and Flinders × Omskiy golozerniy (15.31%). Based on an average of the study years, the drought-resistant and highproductivity hybrid lines were Buloke × Karagadinckiy-6, Fathom × Donezckiy-9, Onslow × Karabalykckiy-43, Onslow × (Karagandinckiy-5 × Аrna), Bass × Karabalykckiy-150, Granal × CMB93H-805-F-1Y-1M-OY-17TRS-OAP, and Granal × CMB89A-380-1M-OGH-105GH-1B-1OY-OAP- 19AP-OAP. These promising genotypes can benefit the development of drought-resistant and highyielding barley cultivars through future breeding programs under prevailing environmental conditions.

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Bystroff, Christopher. "MASKER: improved solvent-excluded molecular surface area estimations using Boolean masks." Protein Engineering, Design and Selection 15, no. 12 (December 2002): 959–65. http://dx.doi.org/10.1093/protein/15.12.959.

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Samanta, Uttamkumar, Ranjit P. Bahadur, and Pinak Chakrabarti. "Quantifying the accessible surface area of protein residues in their local environment." Protein Engineering, Design and Selection 15, no. 8 (August 2002): 659–67. http://dx.doi.org/10.1093/protein/15.8.659.

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Rohan, Zdenek, and Radoslav Matej. "Current Concepts in the Classification and Diagnosis of Frontotemporal Lobar Degenerations: A Practical Approach." Archives of Pathology & Laboratory Medicine 138, no. 1 (January 1, 2014): 132–38. http://dx.doi.org/10.5858/arpa.2012-0510-rs.

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Frontotemporal lobar degenerations are clinically, genetically, and molecularly heterogeneous diseases characterized by mainly frontal and temporal atrophy and affecting behavioral, language, cognitive, and motor functions. The term frontotemporal dementia incorporates 3 distinct clinical syndromes seen in frontotemporal degenerations: behavioral variant of frontotemporal dementia, progressive nonfluent aphasia, and semantic dementia. Progressive supranuclear palsy syndrome, corticobasal syndrome, and motor neuron disease syndrome are also associated with frontotemporal lobar degenerations. The neuropathologic hallmark of frontotemporal lobar degenerations is accumulation of abnormal proteins in the cytoplasm and nuclei of neurons and glial cells. Proteins involved in pathologic processes that represent the basis for frontotemporal lobar degeneration classification are tau protein, transactive response DNA-binding protein of 43 kDa, and “fused in sarcoma” protein. The aim of this review is to provide a summary of practical approaches for neuropathologic diagnostics of the rapidly evolving classifications of frontotemporal lobar degenerations.

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Giannini, Gabriel, and Cynthia C. Nast. "An Organ System–Based Approach to Differential Diagnosis of Amyloid Type in Surgical Pathology." Archives of Pathology & Laboratory Medicine 144, no. 3 (November 7, 2019): 379–87. http://dx.doi.org/10.5858/arpa.2018-0509-ra.

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Context.— Amyloidosis is an uncommon but important entity. A protein-based classification of amyloidosis defines the underlying disease process, directing clinical management and providing prognostic information. However, in routine surgical pathology there often is no attempt to classify amyloid other than staining to determine light chain–associated amyloidosis. Systemic and localized amyloidosis vary with respect to frequency of organ involvement by different amyloid types, and most amyloid proteins have commercial antibodies available for identification. Objective.— To provide a guide for the likelihood of amyloid type by organ system. Data Sources.— Literature review based on PubMed searches containing the word amyloid, specifically addressing the prevalence and significance of amyloid proteins in each organ system other than the brain, and the authors' practice experience. Conclusions.— In patients with amyloidosis, determination of the responsible protein is critical for appropriate patient care. In large subspecialty practices and reference laboratories with experience in using and analyzing relevant immunohistochemistry, most amyloid proteins can be identified with an organ-specific algorithm. Referring to an organ-based algorithm may be helpful in providing clinicians with a more specific differential diagnosis regarding amyloid type to help guide clinical evaluation and treatment. When the protein cannot be characterized, mass spectrometry can be performed to definitively classify the amyloid type.

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Hasselbalch, Hans Carl, Vibe Skov, Thomas Stauffer Larsen, Mads Thomassen, Caroline Riley, Morten Krogh Jensen, Ole Weis Bjerrum, and Torben A. Kruse. "High Expression of Carcinoembryonic Antigen-Related Cell Adhesion Molecule(CEACAM) 6 In Primary Myelofibrosis." Blood 116, no. 21 (November 19, 2010): 4116. http://dx.doi.org/10.1182/blood.v116.21.4116.4116.

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Abstract Abstract 4116 Introduction: Carcinoembryonic antigen-related cell adhesion molecule (CEACAM) 6, also known as non-specific cross-reacting antigen (NCA) or CD66c is a glycosylphosphoinositol (GPI)-linked cell surface protein and a member of the CEA family of proteins. Structurally, this protein shares close homology with CEACAM1, CEACAM7 and CEACAM8. Functionally, CEACAM6 has been implicated in cell adhesion, cellular invasiveness and metastatic behaviour of tumour cells. Expression of CEACAM6 protein has been found in a variety of normal human tissues, including myeloid cells. A key pathophysiological feature of primary myelofibrosis (PMF) is changes in the bone marrow micromilieu, progressive accumulation of connective tissue, pronounced neovascularisation and altered stromal cell adhesion. Consequently, CD34+ cells escape the bone marrow and seed extramedullarily. Being involved in cell adhesion, cellular invasiveness, angiogenesis, and inflammation – all key processes in the pathophysiology of PMF – we hypothesized that CEACAM6 might play an important role in these processes in patients with myelofibrosis. We have assessed gene expression of several CEA genes in patients with PMF and related neoplasms in order to elucidate the significance of CEACAM6 and other members of the CEA family of proteins in these disorders. Patients and Methods: Gene expression microarray studies have been performed on whole blood from control subjects (n=21) and patients with ET (n =19), PV (n=41), and PMF (n=9). Gene expression profiles were generated using Affymetrix HG-U133 2.0 Plus microarrays recognizing 54.675 probe sets (38.500 genes). Total RNA was purified from whole-blood and amplified to biotin-labeled aRNA and hybridized to microarray chips. Results: 20.439, 25.307, 17.417, and 25.421 probe sets were identified to be differentially expressed between controls and patients with ET, PV, PMF, and CPMNs as a whole, respectively (false discovery rate (FDR) adjusted p values < 0.05). Several CEACAM-genes were significantly deregulated. In PMF patients, the CEACAM genes 1, 6 and 8 were significantly upregulated with the highest upregulation of CEACAM6 and CEACAM8 (fold change (FC) 12.5 and 14.0, respectively and FDR adjusted p values 7.71 × 10-7 and 1.48 × 10-5, respectively). Only the CEACAM21 gene was significantly downregulated (FC -1.3 and FDR adjusted p-value 4.14 × 10-7) whereas the other CEACAM-genes tested (3, 4, 5, 7, 19) displayed no significant changes as compared to controls. In ET patients, the CEACAM genes 3, 6, and 7 were significantly upregulated (FC 1.2, 1.8, and 1.1, respectively) and FDR adjusted p values < 0.03). The CEACAM21 gene was significantly downregulated (FC -1.3 and FDR adjusted p-value 0.0004). In PV patients, the CEACAM genes 1, 3, 6 and 7 were significantly upregulated (FC 1.7, 1.2, 1.7, and 1.1, respectively) and FDR adjusted p values 0.0002, 0.0009, 0.0002, and 0.03, respectively. The CEACAM21 gene was significantly downregulated (FC -1.3 and FDR adjusted p-value 4.14×10-5) All other CEACAM-genes showed no significant changes in either ET or PV as compared to controls.When comparing controls with non-PMF-patients, a significant upregulation of the CEACAM genes 1, 3, 6, and 7 were recorded in non-PMF patients (FC 1.5, 1.2, 1.7, and 1.1, respectively; FDR adjusted p values 0.001, 0.0002, 0.002, and 0.02, respectively). The CEACAM19 and CEACAM21 genes were significantly downregulated (FC - 1.1 and -1.4, respectively; adjusted p-values 0.008 and 3.46 × 10-8). Discussion and Conclusions: Using global gene expression profiling, we have found a pronounced deregulation of CEACAM genes, involving highly significant upregulation of the CEACAM genes 6 and 8 in PMF (FCs 12.0 and 14.0, respectively). Upregulation of CEACAM6 was seen in both ET, PV and PMF by far the highest levels being recorded in PMF-patients. Of note, significant upregulation of CEACAM8 (FC 14) was only seen in patients with myelofibrosis. The elevated expression of CEACAMs genes in ET, PV, and PMF may solely reflect neutrophil activation being most exaggerated in patients with PMF in whom the highest CEACAM6 and 8 expression patterns were recorded. Alternatively, the highly elevated gene expression of CEACAM6 and 8 in PMF are molecular markers of clonal expansion and myelofibrotic transformation, implying enhanced proteolytic activity and egress of CD34+ cells into the circulation. Disclosures: No relevant conflicts of interest to declare.

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Acosta, Andres Martin, and ShriHari S. Kadkol. "Mitogen-Activated Protein Kinase Signaling Pathway in Cutaneous Melanoma: An Updated Review." Archives of Pathology & Laboratory Medicine 140, no. 11 (November 1, 2016): 1290–96. http://dx.doi.org/10.5858/arpa.2015-0475-rs.

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The mitogen-activated protein kinase (MAPK) signaling pathway is a cascade of protein kinases that act in a sequential and predominantly linear fashion, albeit displaying some cross talk with other signaling cascades. Mutations in proteins integral to the MAPK signaling pathway are present in more than 50% of cutaneous melanomas. The most frequently mutated protein is v-raf murine sarcoma viral oncogene homolog B (BRAF), followed by neuroblastoma Ras viral oncogene homolog (NRAS). Recently, the development of targeted drugs for the treatment of BRAF-mutant melanoma has led to the widespread implementation of molecular assays for the detection of specific BRAF mutations. There have been some attempts to standardize testing of BRAF mutations, but this has not been achieved so far. Here we provide an updated review on the role of the MAPK signaling pathway in the pathogenesis of cutaneous melanoma, focusing on several different BRAF mutations and their diagnostic and therapeutic implications.

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Templin, Andrew T., Mahnaz Mellati, Raija Soininen, Meghan F. Hogan, Nathalie Esser, J. Josh Castillo, Sakeneh Zraika, Steven E. Kahn, and Rebecca L. Hull. "Loss of perlecan heparan sulfate glycosaminoglycans lowers body weight and decreases islet amyloid deposition in human islet amyloid polypeptide transgenic mice." Protein Engineering, Design and Selection 32, no. 2 (February 2019): 95–102. http://dx.doi.org/10.1093/protein/gzz041.

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Abstract Islet amyloid is a pathologic feature of type 2 diabetes (T2D) that is associated with β-cell loss and dysfunction. These amyloid deposits form via aggregation of the β-cell secretory product islet amyloid polypeptide (IAPP) and contain other molecules including the heparan sulfate proteoglycan perlecan. Perlecan has been shown to bind amyloidogenic human IAPP (hIAPP) via its heparan sulfate glycosaminoglycan (HS GAG) chains and to enhance hIAPP aggregation in vitro. We postulated that reducing the HS GAG content of perlecan would also decrease islet amyloid deposition in vivo. hIAPP transgenic mice were crossed with Hspg2Δ3/Δ3 mice harboring a perlecan mutation that prevents HS GAG attachment (hIAPP;Hspg2Δ3/Δ3), and male offspring from this cross were fed a high fat diet for 12 months to induce islet amyloid deposition. At the end of the study body weight, islet amyloid area, β-cell area, glucose tolerance and insulin secretion were analyzed. hIAPP;Hspg2Δ3/Δ3 mice exhibited significantly less islet amyloid deposition and greater β-cell area compared to hIAPP mice expressing wild type perlecan. hIAPP;Hspg2Δ3/Δ3 mice also gained significantly less weight than other genotypes. When adjusted for differences in body weight using multiple linear regression modeling, we found no differences in islet amyloid deposition or β-cell area between hIAPP transgenic and hIAPP;Hspg2Δ3/Δ3 mice. We conclude that loss of perlecan exon 3 reduces islet amyloid deposition in vivo through indirect effects on body weight and possibly also through direct effects on hIAPP aggregation. Both of these mechanisms may promote maintenance of glucose homeostasis in the setting of T2D.

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Khan, Mohammad Ashhar I., Ulrich Weininger, Sven Kjellström, Shashank Deep, and Mikael Akke. "Adsorption of unfolded Cu/Zn superoxide dismutase onto hydrophobic surfaces catalyzes its formation of amyloid fibrils." Protein Engineering, Design and Selection 32, no. 2 (February 2019): 77–85. http://dx.doi.org/10.1093/protein/gzz033.

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Abstract Intracellular aggregates of superoxide dismutase 1 (SOD1) are associated with amyotrophic lateral sclerosis. In vivo, aggregation occurs in a complex and dense molecular environment with chemically heterogeneous surfaces. To investigate how SOD1 fibril formation is affected by surfaces, we used an in vitro model system enabling us to vary the molecular features of both SOD1 and the surfaces, as well as the surface area. We compared fibril formation in hydrophilic and hydrophobic sample wells, as a function of denaturant concentration and extraneous hydrophobic surface area. In the presence of hydrophobic surfaces, SOD1 unfolding promotes fibril nucleation. By contrast, in the presence of hydrophilic surfaces, increasing denaturant concentration retards the onset of fibril formation. We conclude that the mechanism of fibril formation depends on the surrounding surfaces and that the nucleating species might correspond to different conformational states of SOD1 depending on the nature of these surfaces.

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Ahmad, Shandar, Michael Gromiha, and A. Sarai. "1J1000 Real value prediction of accessible surface area in proteins." Seibutsu Butsuri 42, supplement2 (2002): S54. http://dx.doi.org/10.2142/biophys.42.s54_2.

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Wilson, W. Cris, and Thomas Boland. "Cell and organ printing 1: Protein and cell printers." Anatomical Record 272A, no. 2 (May 6, 2003): 491–96. http://dx.doi.org/10.1002/ar.a.10057.

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Kern, Christine B., Stanley Hoffman, Ricardo Moreno, Brook J. Damon, Russell A. Norris, Edward L. Krug, Roger R. Markwald, and Corey H. Mjaatvedt. "Immunolocalization of chick periostin protein in the developing heart." Anatomical Record Part A: Discoveries in Molecular, Cellular, and Evolutionary Biology 284A, no. 1 (2005): 415–23. http://dx.doi.org/10.1002/ar.a.20193.

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Dees, Ellen, J. Brian Robertson, Mabelle Ashe, Lil M. Pabón-Peña, David Bader, and Richard L. Goodwin. "LEK1 protein expression in normal and dysregulated cardiomyocyte mitosis." Anatomical Record Part A: Discoveries in Molecular, Cellular, and Evolutionary Biology 286A, no. 1 (2005): 823–32. http://dx.doi.org/10.1002/ar.a.20221.

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Dinarvand, Peyman, and Karen A. Moser. "Protein C Deficiency." Archives of Pathology & Laboratory Medicine 143, no. 10 (February 1, 2019): 1281–85. http://dx.doi.org/10.5858/arpa.2017-0403-rs.

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Protein C (PC) deficiency is a heritable or acquired risk factor for thrombophilia, with presentations varying from asymptomatic to venous thromboembolism to neonatal purpura fulminans, a life-threatening disorder. Hereditary PC deficiency is caused by mutation in the PC (PROC) gene located on chromosome 2q14.3. Heterozygous and acquired PC deficiencies are more common than homozygous deficiency. The recommended initial laboratory test measures PC activity using either clot-based or chromogenic methods. There are numerous potential interferences in PC activity testing that may result in either false-positive (falsely low activity) or false-negative (falsely normal or elevated activity) results. In the present review, we discuss common clinical presentations; laboratory testing, with a focus on potential assay interferences; treatment options; and prognosis in patients with PC deficiency.

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Khoor, Andras, and Thomas V. Colby. "Amyloidosis of the Lung." Archives of Pathology & Laboratory Medicine 141, no. 2 (February 1, 2017): 247–54. http://dx.doi.org/10.5858/arpa.2016-0102-ra.

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Context.—Amyloidosis is a heterogeneous group of diseases characterized by the deposition of congophilic amyloid fibrils in the extracellular matrix of tissues and organs. To date, 31 fibril proteins have been identified in humans, and it is now recommended that amyloidoses be named after these fibril proteins. Based on this classification scheme, the most common forms of amyloidosis include systemic AL (formerly primary), systemic AA (formerly secondary), systemic wild-type ATTR (formerly age-related or senile systemic), and systemic hereditary ATTR amyloidosis (formerly familial amyloid polyneuropathy). Three different clinicopathologic forms of amyloidosis can be seen in the lungs: diffuse alveolar-septal amyloidosis, nodular pulmonary amyloidosis, and tracheobronchial amyloidosis. Objective.—To clarify the relationship between the fibril protein–based amyloidosis classification system and the clinicopathologic forms of pulmonary amyloidosis and to provide a useful guide for diagnosing these entities for the practicing pathologist. Data Sources.—This is a narrative review based on PubMed searches and the authors' own experiences. Conclusions.—Diffuse alveolar-septal amyloidosis is usually caused by systemic AL amyloidosis, whereas nodular pulmonary amyloidosis and tracheobronchial amyloidosis usually represent localized AL amyloidosis. However, these generalized scenarios cannot always be applied to individual cases. Because the treatment options for amyloidosis are dependent on the fibril protein–based classifications and whether the process is systemic or localized, the workup of new clinically relevant cases should include amyloid subtyping (preferably with mass spectrometry–based proteomic analysis) and further clinical investigation.

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Gill, Matthew, and Michelle E. McCully. "Molecular dynamics simulations suggest stabilizing mutations in a de novo designed α/β protein." Protein Engineering, Design and Selection 32, no. 7 (July 2019): 317–29. http://dx.doi.org/10.1093/protein/gzaa005.

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Abstract Designing functional proteins that can withstand extreme heat is beneficial for industrial and protein therapeutic applications. Thus, elucidating the atomic-level determinants of thermostability is a major interest for rational protein design. To that end, we compared the structure and dynamics of a set of previously designed, thermostable proteins based on the activation domain of human procarboxypeptidase A2 (AYEwt). The mutations in these designed proteins were intended to increase hydrophobic core packing and inter-secondary-structure interactions. To evaluate whether these design strategies were successfully deployed, we performed all-atom, explicit-solvent molecular dynamics (MD) simulations of AYEwt and three designed variants at both 25 and 100°C. Our MD simulations agreed with the relative experimental stabilities of the designs based on their secondary structure content, Cα root-mean-square deviation/fluctuation, and buried-residue solvent accessible surface area. Using a contact analysis, we found that the designs stabilize inter-secondary structure interactions and buried hydrophobic surface area, as intended. Based on our analysis, we designed three additional variants to test the role of helix stabilization, core packing, and a Phe → Met mutation on thermostability. We performed the additional MD simulations and analysis on these variants, and these data supported our predictions.

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Arnason, Thomas, Heidi L. Sapp, Daniel Rayson, Penelope J. Barnes, Magdalena Drewniak, Bassam A. Nassar, and Weei-Yuarn Huang. "Loss of Expression of DNA Mismatch Repair Proteins Is Rare in Pancreatic and Small Intestinal Neuroendocrine Tumors." Archives of Pathology & Laboratory Medicine 135, no. 12 (December 1, 2011): 1539–44. http://dx.doi.org/10.5858/arpa.2010-0560-oa.

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Context.—Two recent studies have identified a high rate of microsatellite instability (MSI) in pancreatic neuroendocrine tumors (pNETs). Microsatellite instability is rare in small intestinal neuroendocrine tumors (NETs). It is unclear why there is discordance in the frequency of MSI in the 2 studies of pNETs and why this mechanism is comparatively rare in small intestinal tumors. Loss of expression of DNA mismatch repair (MMR) proteins, which is known to correlate strongly with MSI, is not well studied in pancreatic or small intestinal NETs. Objective.—To determine if there is loss of expression of MMR protein expression in pancreatic or small intestinal NETs. Design.—Sixty-nine patients (31 male, 38 female; mean age, 59.2 years) were identified who had a resection for a primary pancreatic (n = 35) or primary small intestinal (n = 34) NET during an 18-year period. Immunohistochemical stains for MLH1, MSH2, MSH6, and PMS2 were applied to archived tissue from all cases. All pNETs with adequate tissue (n = 32) were also assessed by MSI analysis. Results.—There was preserved expression of MLH1, MSH2, MSH6, and PMS2 in all 35 pNETs. Of 32 pNETs tested by polymerase chain reaction, 28 were microsatellite stable and DNA did not amplify in 4. In 34 small intestinal NETs, 2 cases had indeterminate MLH1 and 1 case had indeterminate PMS2 expression. The remainder had intact MMR protein expression. Conclusion.—Defects in DNA MMR proteins are rare in pancreatic and small intestinal NETs, raising doubt that MSI plays a significant role in the pathogenesis of these tumors.

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Sun, S., and R. Parthasarathy. "Protein sequence and structure relationship ARMA spectral analysis: application to membrane proteins." Biophysical Journal 66, no. 6 (June 1994): 2092–106. http://dx.doi.org/10.1016/s0006-3495(94)81004-5.

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Somi, Semir, Anita A. M. Buffing, Antoon F. M. Moorman, and Maurice J. B. Van Den Hoff. "Expression of bone morphogenetic protein-10 mRNA during chicken heart development." Anatomical Record 279A, no. 1 (2004): 579–82. http://dx.doi.org/10.1002/ar.a.20052.

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Kamau, Edwin, Richard Bonneau, and Xiang-Peng Kong. "Computational-guided determination of the functional role of 447-52D long CDRH3." Protein Engineering, Design and Selection 31, no. 12 (December 1, 2018): 479–87. http://dx.doi.org/10.1093/protein/gzz007.

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Abstract447-52D (447) is a human monoclonal antibody that recognizes a conserved epitope in the crown region of the third variable loop (V3) of HIV-1 gp120, and like many anti-HIV-1 antibodies with broad neutralization capabilities, it has a long heavy-chain complementarity determining region (CDRH3). Here, we use a combination of computational mutagenesis and modeling in tandem with fluorescence polarization assays to interrogate the molecular basis of 447 CDRH3 length and the individual contribution of selected CDRH3 residues to affinity. We observe that 447 CDRH3 length provides a large binding surface area and the best enthalpic contributions derived from hydrophobic packing, main-chain hydrogen bonds, electrostatic and van der Waals interactions. We also found out that CDRH3 residue Try100I is critical to 447 binding affinity.

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Takeuchi, Koichi, Amornpan Sereemaspun, Takeshi Inagaki, Yoji Hakamata, Takashi Kaneko, Takashi Murakami, Masafumi Takahashi, Eiji Kobayashi, and Shigeo Ookawara. "Morphologic characterization of green fluorescent protein in embryonic, neonatal, and adult transgenic rats." Anatomical Record 274A, no. 2 (September 8, 2003): 883–86. http://dx.doi.org/10.1002/ar.a.10111.

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Alibardi, Lorenzo, and Mattia Toni. "Immunolocalization and characterization of cornification proteins in snake epidermis." Anatomical Record Part A: Discoveries in Molecular, Cellular, and Evolutionary Biology 282A, no. 2 (2005): 138–46. http://dx.doi.org/10.1002/ar.a.20153.

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Litvin, Judith, Shimei Zhu, Russell Norris, and Roger Markwald. "Periostin family of proteins: Therapeutic targets for heart disease." Anatomical Record Part A: Discoveries in Molecular, Cellular, and Evolutionary Biology 287A, no. 2 (2005): 1205–12. http://dx.doi.org/10.1002/ar.a.20237.

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Fernández-Quintero, Monica L., Johannes R. Loeffler, Franz Waibl, Anna S. Kamenik, Florian Hofer, and Klaus R. Liedl. "Conformational selection of allergen-antibody complexes—surface plasticity of paratopes and epitopes." Protein Engineering, Design and Selection 32, no. 11 (November 2019): 513–23. http://dx.doi.org/10.1093/protein/gzaa014.

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Abstract Antibodies have the ability to bind various types of antigens and to recognize different antibody-binding sites (epitopes) of the same antigen with different binding affinities. Due to the conserved structural framework of antibodies, their specificity to antigens is mainly determined by their antigen-binding site (paratope). Therefore, characterization of epitopes in combination with describing the involved conformational changes of the paratope upon binding is crucial in understanding and predicting antibody-antigen binding. Using molecular dynamics simulations complemented with strong experimental structural information, we investigated the underlying binding mechanism and the resulting local and global surface plasticity in the binding interfaces of distinct antibody-antigen complexes. In all studied allergen-antibody complexes, we clearly observe that experimentally suggested epitopes reveal less plasticity, while non-epitope regions show high surface plasticity. Surprisingly, the paratope shows higher conformational diversity reflected in substantially higher surface plasticity, compared to the epitope. This work allows a visualization and characterization of antibody-antigen interfaces and might have strong implications for antibody-antigen docking and in the area of epitope prediction.

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Brugge, Jeroen, Guido Tans, Jan Rosing, and Elisabetta Castoldi. "Protein S levels modulate the activated protein C resistance phenotype induced by elevated prothrombin levels." Thrombosis and Haemostasis 95, no. 02 (2006): 236–42. http://dx.doi.org/10.1160/th05-08-0582.

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SummaryElevated plasma prothrombin levels, due to the prothrombin 20210 G/A mutation or to acquired causes, area risk factor for venous thrombosis,partly because of prothrombin-mediated inhibition of the protein C anticoagulant pathway and consequent activated proteinC (APC) resistance. We determined the effect of plasma prothrombin concentration on the APC resistance phenotype and evaluated the role of protein S levels asa modulating variable. The effect of prothrombin and protein S levels on APC resistance was investigated in reconstituted plasma systems and in a population of healthy individuals using both the aPTT-based and the thrombin generation-based APC resistance tests. In reconstituted plasma, APC resistance increased at increasing prothrombin concentration in both assays. Enhanced APC resistance was caused by the effect of prothrombin on the clotting time in the absence of APC in the aPTT-based test, and on thrombin formation in the presence of APC in the thrombin generation-based test. In plasma from healthy individuals prothrombin levels were highly correlated to protein S levels. Since prothrombin and proteinS had opposite effects on the APC resistance phenotype, the prothrombin/protein S ratio was a better predictor of APC resistance than the levels of either protein alone. Prothrombin titrations in plasmas containing different amounts of proteinS confirmed that proteinS levels modulate the ability of prothrombin to induce APC resistance. These findings suggest that carriers of the prothrombin 20210 G/A mutation, who have a high prothrombin/protein S ratio, may experience a higher thrombosis risk than non-carriers with comparable prothrombin levels.

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Weber, Marion, Konstantin Chernov, Hilkka Turakainen, Gerd Wohlfahrt, Maria Pajunen, Harri Savilahti, and Jussi Jäntti. "Mso1p Regulates Membrane Fusion through Interactions with the Putative N-Peptide–binding Area in Sec1p Domain 1." Molecular Biology of the Cell 21, no. 8 (April 15, 2010): 1362–74. http://dx.doi.org/10.1091/mbc.e09-07-0546.

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Sec1p/Munc18 (SM) family proteins regulate SNARE complex function in membrane fusion through their interactions with syntaxins. In addition to syntaxins, only a few SM protein interacting proteins are known and typically, their binding modes with SM proteins are poorly characterized. We previously identified Mso1p as a Sec1p-binding protein and showed that it is involved in membrane fusion regulation. Here we demonstrate that Mso1p and Sec1p interact at sites of exocytosis and that the Mso1p–Sec1p interaction site depends on a functional Rab GTPase Sec4p and its GEF Sec2p. Random and targeted mutagenesis of Sec1p, followed by analysis of protein interactions, indicates that Mso1p interacts with Sec1p domain 1 and that this interaction is important for membrane fusion. In many SM family proteins, domain 1 binds to a N-terminal peptide of a syntaxin family protein. The Sec1p-interacting syntaxins Sso1p and Sso2p lack the N-terminal peptide. We show that the putative N-peptide binding area in Sec1p domain 1 is important for Mso1p binding, and that Mso1p can interact with Sso1p and Sso2p. Our results suggest that Mso1p mimics N-peptide binding to facilitate membrane fusion.

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El-Sharaby, Ashraf, Katsura Ueda, and Satoshi Wakisaka. "Immunohistochemical distribution of growth-associated protein 43 (GAP-43) in developing rat nasoincisor papilla." Anatomical Record 277A, no. 2 (2004): 370–83. http://dx.doi.org/10.1002/ar.a.20026.

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Egashira, Katsuko, Kiyomasa Nishii, Kei-Ichiro Nakamura, Madoka Kumai, Sachio Morimoto, and Yosaburo Shibata. "Conduction abnormality in gap junction protein connexin45-deficient embryonic stem cell-derived cardiac myocytes." Anatomical Record 280A, no. 2 (October 2004): 973–79. http://dx.doi.org/10.1002/ar.a.20110.

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de Castro, María Pilar, Amelia Aránega, and Diego Franco. "Protein distribution of Kcnq1, Kcnh2, and Kcne3 potassium channel subunits during mouse embryonic development." Anatomical Record Part A: Discoveries in Molecular, Cellular, and Evolutionary Biology 288A, no. 3 (2006): 304–15. http://dx.doi.org/10.1002/ar.a.20312.

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Day, Austin L., Per Greisen, Lindsey Doyle, Alberto Schena, Nephi Stella, Kai Johnsson, David Baker, and Barry Stoddard. "Unintended specificity of an engineered ligand-binding protein facilitated by unpredicted plasticity of the protein fold." Protein Engineering, Design and Selection 31, no. 10 (October 1, 2018): 375–87. http://dx.doi.org/10.1093/protein/gzy031.

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Abstract Attempts to create novel ligand-binding proteins often focus on formation of a binding pocket with shape complementarity against the desired ligand (particularly for compounds that lack distinct polar moieties). Although designed proteins often exhibit binding of the desired ligand, in some cases they display unintended recognition behavior. One such designed protein, that was originally intended to bind tetrahydrocannabinol (THC), was found instead to display binding of 25-hydroxy-cholecalciferol (25-D3) and was subjected to biochemical characterization, further selections for enhanced 25-D3 binding affinity and crystallographic analyses. The deviation in specificity is due in part to unexpected altertion of its conformation, corresponding to a significant change of the orientation of an α-helix and an equally large movement of a loop, both of which flank the designed ligand-binding pocket. Those changes led to engineered protein constructs that exhibit significantly more contacts and complementarity towards the 25-D3 ligand than the initial designed protein had been predicted to form towards its intended THC ligand. Molecular dynamics simulations imply that the initial computationally designed mutations may contribute to the movement of the helix. These analyses collectively indicate that accurate prediction and control of backbone dynamics conformation, through a combination of improved conformational sampling and/or de novo structure design, represents a key area of further development for the design and optimization of engineered ligand-binding proteins.

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Jackson, Richard M., and Michael J. E. Sternberg. "Protein surface area defined." Nature 366, no. 6456 (December 1993): 638. http://dx.doi.org/10.1038/366638b0.

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Fabian, Carol J., Teresa A. Phillips, and Bruce F. Kimler. "Abstract P1-10-04: AGR2, an estrogen response gene associated with tamoxifen resistance, is modulated by acolbifene in premenopausal women at high risk for development of breast cancer." Cancer Research 82, no. 4_Supplement (February 15, 2022): P1–10–04—P1–10–04. http://dx.doi.org/10.1158/1538-7445.sabcs21-p1-10-04.

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Abstract Anterior Gradient 2 is an estrogen early response gene (AGR2) and protein (AGR-2). High expression is associated with endoplasmic reticulum stress and endocrine therapy resistance. Developmentally, AGR2 is associated with estrogen-mediated epithelial proliferation and lobuloalveolar development. In the adult, AGR2 is upregulated by inflammatory and metabolic stress signaling from NFKB, HSP90, IGFR-1, and FOXA1, in addition to estrogen bound to its receptor. The Selective Estrogen Receptor Modulator (SERM) Full dose tamoxifen has been reported to upregulate AGR2 in breast cancer but Selective Estrogen Receptor Down Regulators (SERDs) and aromatase inhibitors do not. AGR-2 is also a secreted protein, with increased tumor levels associated with metastases and decreased disease-free survival in tamoxifen-treated patients. We assessed AGR2 expression in reserved benign breast tissue from baseline and off-study specimens acquired by random periareolar fine needle aspiration (RPFNA) of premenopausal women at high risk for development of breast cancer who had participated in an early phase prevention trial of the SERM acolbifene (20 mg daily for 6 months). This pilot had demonstrated reduced Ki-67 and down-regulation of several estrogen response genes (Fabian et al. Ca Prev Res 2015). Methods Total RNA was extracted from aliquots of frozen benign breast tissue using TRIzol LS (Life Technologies) and purified using RNeasy MinElute Cleanup Kit (Qiagen). RNA was amplified using MessageAmpII aRNA amplification kit (Life Technologies) and reverse transcribed to cDNA using SMARTScribe Reverse Transcriptase (Takara Bio USA, Inc.) and random nonamer primers. Real-time quantitative PCR (qPCR) was performed using hydrolysis probes with baseline and postintervention specimens assessed together. PCR reactions were run on an Applied Biosystems Prism 7000 Sequence Detection System. The cycle threshold mean value for each transcript (from duplicate assays per specimen) was normalized using three reference transcripts, plus two epithelial cell transcripts. Relative levels of each transcript were calculated using the ΔΔCt method. The ratio (postintervention: baseline) of final values indicated upregulation (value > 1) or downregulation (value < 1). Results There were 17 available paired specimens for analysis for AGR2 gene expression which was downregulated in 13 with nine by more than a 50% reduction; for the four cases of up-regulation, three were increased by more than two-fold (p=0.076, Wilcoxon signed ranks test). Several estrogen response genes (TFF1, PGR, and the ratio of ESR1:ESR2) exhibited significant down-regulation (p≤0.007). Further, there was no evidence of linear correlation (p>0.28; Spearman’s rho) between change in AGR2 and any of these other estrogen response genes. Lastly, when an Estrogen Response Gene Index (ERGI) was constructed using the average log2(fold change) for TFF1, PGR, and the ratio of ESR1:ESR2, down regulation was observed in 16 of the 17 paired specimens with only one increase. ERGI and AGR2 change indicate favorable modulation by acolbifene and appear to provide independent information. Conclusions These results suggest that change in expression of benign breast AGR2 might be a useful addition to change in expression of other classic estrogen response genes in evaluating the potential of novel SERMs such as acolbifene compared to standard SERMs like tamoxifen in early phase prevention trials. Citation Format: Carol J. Fabian, Teresa A. Phillips, Bruce F. Kimler. AGR2, an estrogen response gene associated with tamoxifen resistance, is modulated by acolbifene in premenopausal women at high risk for development of breast cancer [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P1-10-04.

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Neill, Stewart G., Debra F. Saxe, Michael R. Rossi, Matthew J. Schniederjan, and Daniel J. Brat. "Genomic Analysis in the Practice of Surgical Neuropathology: The Emory Experience." Archives of Pathology & Laboratory Medicine 141, no. 3 (March 1, 2017): 355–65. http://dx.doi.org/10.5858/arpa.2016-0276-sai.

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The evaluation of central nervous system tumors increasingly relies on molecular genetic methods to aid in classification, offer prognostic information, and predict response to therapy. Available assays make it possible to assess genetic losses, amplifications, translocations, mutations, or the expression levels of specific gene transcripts or proteins. Current molecular diagnostics frequently use a panel-based approach and whole genome analysis, and generally rely either on DNA sequencing or on hybridization-based methodologies, such as those used in cytogenomic microarrays. In some cases, immunohistochemistry can be used as a surrogate for genetic analysis when the mutation of interest consistently results in overexpression or underexpression of a known protein product. In surgical neuropathology practice, the diagnostic workup of diffuse gliomas, medulloblastomas, low-grade circumscribed gliomas, as well as other diseases, now routinely incorporates the results of genomic studies. Here we summarize our institution's current approach to diagnostic surgical neuropathology, using these contemporary molecular diagnostic applications.

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Valbuena, Teresa, Marta Reche, Guadalupe Marco, Inmaculada Toboso, Anna Ringauf, Israel J. Thuissard-Vasallo, Daniel Lozano-Ojalvo, Mónica Martínez-Blanco, and Elena Molina. "Storage Proteins Are Driving Pediatric Hazelnut Allergy in a Lipid Transfer Protein-Rich Area." Foods 10, no. 10 (October 15, 2021): 2463. http://dx.doi.org/10.3390/foods10102463.

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Oral food challenge (OFC) remains the gold standard for the diagnosis of food allergies. However, this test is not without risks, given that severe allergic reactions can be triggered while it is conducted. The purpose of this study is to identify potential demographic variables, clinical characteristics of the patients and biomarkers that may be associated with severe reactions during the hazelnut oral challenge test. The sample included 22 children allergic to hazelnut who underwent a tree nut skin prick test (SPT), specific IgE (sIgE) to hazelnut, component-resolved diagnosis (CRD) with different hazelnut allergens (Cor a 1, Cor a 8, Cor a 9, Cor a 11, Cor a 14), and a single-blind placebo-controlled challenge with hazelnut. A statistically significant relationship was found between the severity of the reaction and the highest values of sIgE to hazelnut, Cor a 11 and Cor a 14, cumulative symptom-triggering dose and sunflower seed sensitization. The use of the CRD is a useful tool to identify patients at higher risk of developing a severe reaction. In this pediatric population sample from Spain, storage proteins were confirmed to be most involved in hazelnut allergy and the development of severe reactions.

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Journal articles on the topic 'ArnA Protein'

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